HCR2 restricts crossover formation via transcriptional repression of HEI10 in Arabidopsis thaliana

Abstract

Meiotic DSBs (DNA double strand break sites) are induced by DNA topoisomerase II-like complexes. The repair of DSBs leads to a reciprocal crossover or a non-crossover via different DNA repair pathways. Crossover number is limited to ~1–3 along chromosomes and one crossover restricts formation of closely spaced another crossover along the same chromosome. Approximately 80–85% crossovers are interfering and dependent on ZMM proteins (ZIP4, MSH4, MSH5, MER3, HEI10, SHOC1, PTD, MLH1, MLH3), while 10–15% of crossovers are non-interfering and formed by MUS81 resolvase. Genetic disruption of FANCM, RECQ4 and FIGL1 genes increases non-interfering crossovers in plants. However, how the formation of interfering crossovers is restricted remains largely unexplored. We here isolated hcr2 (higher crossover rate 2) mutant via a forward genetic screen using fluorescent seed-based system in Arabidopsis that enables to measure crossover rate in individual plants. The hcr2 mutant displays increased crossover frequency in chromosome arms and similar crossover rates around centromeres, compared to wild type plant. HCR2 gene encodes a heat shock factor binding protein that is known as a negative transcriptional regulator in heat shock response. The hcr2 mutation increases the transcript level of an E3 ligase gene HEI10, which promotes interfering-crossovers in a dosage dependent manner. Together, our data reveal a novel mechanism of limiting interfering-crossovers via a heat shock transcriptional regulator.